Evidence map›Paper›PMID 25274827›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

GluA1 phosphorylation contributes to postsynaptic amplification of neuropathic pain in the insular cortex.

Shuang Qiu, Ming Zhang, Yan Liu, Yanyan Guo, Huan Zhao, Qian Song, Minggao Zhao, Richard L Huganir, Jianhong Luo, Hui Xu and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
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  13. The Role of the Insular Cortex in Pain.International journal of molecular sciences · 2023
    Review
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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Shuang QiuDepartment of Neurobiology, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University School of Medicine, Hangzhou 310058, China, Center for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China, Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada, M5S 1A8, and.
Ming ZhangCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China, Institute of Neurosciences, Fourth Military Medical University, Xi'an 710032, China.
Yan LiuInstitute of Neurosciences, Fourth Military Medical University, Xi'an 710032, China.
Yanyan GuoCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Huan ZhaoCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China, Institute of Neurosciences, Fourth Military Medical University, Xi'an 710032, China.
Qian SongCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Minggao ZhaoCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Richard L HuganirDepartment of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Jianhong LuoDepartment of Neurobiology, Key Laboratory of Medical Neurobiology of the Ministry of Health of China, Zhejiang University School of Medicine, Hangzhou 310058, China.
Hui XuCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China, Institute of Neurosciences, Fourth Military Medical University, Xi'an 710032, China, min.zhuo@utoronto.ca xubz@fmmu.edu.cn.
Min ZhuoCenter for Neuron and Disease, Frontier Institutes of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China, Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada, M5S 1A8, and min.zhuo@utoronto.ca xubz@fmmu.edu.cn.
Xi'an Jiaotong University · CNAir Force Medical University · CNJohns Hopkins University · US

Funding

PDZ DOMAINS AND EXCITATORY SYNAPTIC FUNCTIONR01NS036715 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1997 to 2020
$8.6M
NINDS NIH HHS R01 NS036715
6 · The paper itself

Abstract

Long-term potentiation of glutamatergic transmission has been observed after physiological learning or pathological injuries in different brain regions, including the spinal cord, hippocampus, amygdala, and cortices. The insular cortex is a key cortical region that plays important roles in aversive learning and neuropathic pain. However, little is known about whether excitatory transmission in the insular cortex undergoes plastic changes after peripheral nerve injury. Here, we found that peripheral nerve ligation triggered the enhancement of AMPA receptor (AMPAR)-mediated excitatory synaptic transmission in the insular cortex. The synaptic GluA1 subunit of AMPAR, but not the GluA2/3 subunit, was increased after nerve ligation. Genetic knock-in mice lacking phosphorylation of the Ser845 site, but not that of the Ser831 site, blocked the enhancement of the synaptic GluA1 subunit, indicating that GluA1 phosphorylation at the Ser845 site by protein kinase A (PKA) was critical for this upregulation after nerve injury. Furthermore, A-kinase anchoring protein 79/150 (AKAP79/150) and PKA were translocated to the synapses after nerve injury. Genetic deletion of adenylyl cyclase subtype 1 (AC1) prevented the translocation of AKAP79/150 and PKA, as well as the upregulation of synaptic GluA1-containing AMPARs. Pharmacological inhibition of calcium-permeable AMPAR function in the insular cortex reduced behavioral sensitization caused by nerve injury. Our results suggest that the expression of AMPARs is enhanced in the insular cortex after nerve injury by a pathway involving AC1, AKAP79/150, and PKA, and such enhancement may at least in part contribute to behavioral sensitization together with other cortical regions, such as the anterior cingulate and the prefrontal cortices.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAnimalsCerebral CortexDisease Models, AnimalEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA AntagonistsIn Vitro TechniquesMaleMembrane PotentialsMiceMice, Inbred C57BLMice, TransgenicMutationNeuralgiaPhosphorylation6-Cyano-7-nitroquinoxaline-2,3-dioneEnzyme InhibitorsExcitatory Amino Acid AntagonistsGABA AntagonistsPicrotoxinReceptors, AMPASodium Channel BlockersTetrodotoxinGluA1insular cortexmouseneuropathic painphosphorylationPKA

Identifiers

PMID25274827
PMCPMC4340970
OpenAlexW2058406386

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.